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LUNG + RENAL STEP 2 > Renal 1 > Flashcards

Renal 1 Flashcards

1
Q

Renal tubular defects - types

A
  1. Fanconi syndrome
  2. Bartter syndrome
  3. Gitelman syndrome
  4. Liddle syndrome
  5. Syndrome of apparent minelocorticoid excess
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2
Q

Fanconi syndrome - pathophysiology / results in

A

Generalized reabsorptive defect in early proximal convoluted tubule –> increased amino acids, glucose, HCO3- and PO4- – Metabolic acidosis (proximal renal tubular acidosis)

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3
Q

causes of Fanconi syndrome

A
  1. hereditary defects (Wilson disease, tyrosinemia, glycogen storage disease, cystinosis)
  2. iscemia
  3. multiple myeloma
  4. nephrotoxins/drugs (expired tetracyclines, ifosfamide, cisplatin, tenofovir, lead poisoning)
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4
Q

Bartter syndrome - pathophysiology (and result in)

A

Reabsorptive defect in thick ascending loop oh Henle
–> affects Na+/K+/2CL- cotransporter –>
1. hypokalemia
2. metabolic alkalosis
3. hypercalciuria
LIKE LOOP DIURETICS

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5
Q

Gitelman syndrome - pathophysiology (results in)

A 
Reabsosptive defect in Distal convoluted tubule 
LIKE THIAZIDE
1. hypokalemia
2. hypomagnesia
3. metabolic alkalosis
4. hypocalciuria
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6
Q

Gitelman syndrome vs Barrter syndrome according to severity

A

Barrter is more severe

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7
Q

Liddle syndrome - pathophysiology

A

Gain of function mutation –> increased Na+ reabsorption in collecting tubules (high activity of epithelial channel)

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8
Q

situation that mimics Liddle syndrome

A

hyperaldosternism (but aldosterone is nearly undetectable)

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9
Q

Liddle syndrome –> ….. (result in)

A
  1. hypertension
  2. hypokalemia
  3. metabolic alkalosis
  4. low aldosterone
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10
Q

Liddle syndrome - mode of inheritance / treatment

A

AD

amiloride

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11
Q

Syndrome of Apparent Mineralocorticoid excess - pathophysiology

A

hereditary deficiency of 11β-hydroxysteroid dehydrogenase which normally converts cortisol (can activate mineralocorticoid receptors) to cortizone (inactivate on mineralocorticoid receptors) in cell containing mineralocorticoid receptors –> increased mineralocorticoid activity

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12
Q

Syndrome of Apparent Mineralocorticoid excess - manifestations

A
  1. hypertension
  2. hypokalemia
  3. metabolic alkalosis
  4. low serum aldosterone levels
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13
Q

P02, PCO2, HCO3-, ph - normal ranges

A

PO2: 75-105 mm Hg
PCO2: 33-44 mm Hg
HCO3-: 22-28 mEq/L
pH: 7.35-7.45

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14
Q

Winters formula?? is a formula used to evaluate

A

respiratory compensation in a metabolic acidosis

PCO2=1.5 (HCO3-) + 8 +/- 2

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15
Q

Winters formula - explanation

A

If measured PCO2 is bigger than predicted PCO2 –> concominant respiratory acidosis
If measured PCO2 is smaller than predicted –> concomitant respiratory alkalosis

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16
Q

Metabolic alkalosis - DDx

A
  1. loop diuretics
  2. vomiting
  3. antiacids
  4. hyperaldosteronism
  5. thiazide use
  6. Hypokalemia
  7. several renal tubular defects
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17
Q

Respiratory alkalosis - DDx

A

Hyperventilation:

  1. Hysteria
  2. Hypoxemia (eg. high altitude)
  3. Pulmoary embolism
  4. Tumor
  5. salicylates (early)
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18
Q

Respiratory acidosis - DDx

A

Hypoventilation:

  1. Airway obstruction
  2. Acute lung disease
  3. Chronic lung disease
  4. Opioids/sedatives
  5. weakening of respiratory muscles
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19
Q

Metabolic acidosis - next step

A

Check anion gap = Na+ - (CL+HCO3-):
more than 12 –> anion gap metabolic acidosis
8-12 –> normal anion gap metabolic acidosis

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20
Q

anion gap metabolic acidosis - DDx

A
  1. Methanol (formic acid)
  2. Uremia
  3. Diabetic ketoacidosis
  4. Propylene glycol
  5. Iron tablets
  6. ISONIAZIDE
  7. Lactic acidosis
  8. Ethylene glycol (–> oxalic acid)
  9. Salicilates (late)
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21
Q

normal anion gap metabolic acidosis - DDx

A
  1. Hyperalimentation (artificial supply of nutrients, typically intravenously)
  2. Addison disease
  3. Renal tubular acidosis
  4. Diarrhea
  5. Acetazolamide
  6. Spironolactone
  7. saline infusion
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22
Q

Renal tubular acidosis - types

A
  1. Distal tubular acidosis (type 1)
  2. Proximal renal tubular acidosis (type 2)
  3. Combined proximal and distal renal tubular acidosis (type 3)
  4. Hyperkalemic renal tubular acidosis (type 4)
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23
Q

Metabolic acidosis - predicted compensatory response

A

1 meq/L decrease in HCO3- –> 1.3 mmHg decrease in PCO2

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24
Q

Metabolic alkalosis - predicted compensatory response

A

1 meq/L increase in HCO3- –> 0.7 mmHg increase in PCO2

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25
Q

Respiratory acidosis - predicted compensatory response

A

acute: 1 mmHg increase in PCO2 –> 0.1 meg/L increase in HCO3-
chronic: 1 mmHg increase in PCO2 –> 0.4 meq/L increase in HCO3-

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26
Q

Respiratory alkalosis - predicted compensatory response

A

acute: 1 mmHg decrease in PCO2 –> 0.2 meq/L decrease in HCO3-
chronic: 1mmHg decrease in PCO2 –> 0.4 meg/L decrease in HCO3-

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27
Q

Renal cell carcinoma - risk factors

A
  1. Smoking
  2. obesity
  3. gene deletion of chromosome 3 (sporadic or inheritance as von Hippel-Lindau
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28
Q

Renal cell carcinoma - paraneoplastic syndromes

A
  1. EPO
  2. ACTH
  3. PTHrP
  4. RENIN
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29
Q

Renal cell carcinoma - prognosis? (why)

A

poor:

  1. Resistant to chemotherapy and radiation therapy
  2. Silent cancer –> comonly presents as a metastatic neoplasm
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30
Q

Renal oncocytoma - clinical manifestations

A
  1. painless hematuria
  2. flank pain
  3. abdominal mass
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31
Q

Renal oncocytoma - treatment

A

often resected to exclude malignancy

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32
Q

Squamous cell carcinoma of the bladder - clinical manifestation

A

painless hematuria

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33
Q

Squamous cell carcinoma of the bladder - risk factors

A
  1. Schistosoma haematobium infection (Middle East)
  2. Chrinic cystitis
  3. smoking
  4. chronic nephrolithiasis
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34
Q

Transition cell carcinoma - manifestations

A

painless hematuria

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35
Q

Calcium oxalate stones are precipitated by (beside low ph)

A
  1. ethylene glycol (antifreeze) ingestion
  2. vitamin C abuse
  3. malabsorption (Crohn disease)
  4. hypocitraturia –> low ph
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36
Q

kidney calcium stone treatment

A

calcium oxalate –> thiazides, citrate, low-sodium diet

calcium phosphate –> thiazides

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37
Q

Ammonium magnesium phosphate stone (sturvite) are caused by

A

infection with urease + bugs (eg. Proteus mirabilis, Staphylococcus saprophyticus, Klebsiella) that hydrolize urea to ammonia –> urina alkalization

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38
Q

Ammonium magnesium phosphate stones (sturvite) - treatment

A
  1. eradication of underling infection

2. surgical removal of stone

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39
Q

Uric acid stones - risk factors

A
  1. low sodium diet
  2. alkalinization of urine
  3. chelating agents if refractory
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40
Q

kidney stones - types and urine crystals

A
  1. Calcium oxalate –> shaped like envelope or dumbbell
  2. Caclicum phosphate –> wedge-shaped prism
  3. Ammonium magnesium phosphate –> coffin lid
  4. Uric acid –> Rhomboid or rosettes
  5. Cystine –> hexagonal
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41
Q

Urinary incontinence - types

A
  1. Stress incontinence
  2. Urgency incontinence
  3. Mixed incontinence
  4. Overflow incontinence
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42
Q

urinary Stress incontinence - mechanism

A

Outlet incompetence (urethral hypermodility or intrinsic sphincteric deficiency –> leak with high intra-abdominal pressure (eg. sneezing, lifting)

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43
Q

urinary Stress incontinence - increased risk with

A

obesity
vaginal delivery
prostate surgery

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44
Q

urinary Stress incontinence - management

A

kegel exercise, weight loss. pessaries

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45
Q

urinary Urgency incontinence - mechanism

A

Overactive bladder (detrusor instability) –> leak with urge to void immediately

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46
Q

urinary Urgency incontinence - treatment

A
  1. pelvic floor muscle strengthening (Kegel) exercise
  2. bladder training (timed voiding, distraction and relaxation techniques)
  3. antimuscarinics (oxybutynin)
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47
Q

Overflow incontinence - mechanism

A

incomplete emptying (detrusor underactivity - weak to emoty the bladder or outlet obstruction) –> leak with overfilling –> increased postvoid residual (urinary retention) on cathetirization or ultrasound

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48
Q

Overflow incontinence - treatment

A 
catherterization
relieve obstruction (α-blockers for BPH)
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49
Q

3 MCC of UTI (in order)

A
  1. E. Coli
  2. S. saprophyticus
  3. Klebsiella pneumoniae
50
Q

UTI - diagnostic markers

A
    • leukocyte esterase –> WBC activity
    • Nitrate test –> reduction of urinary nitrates by bacterial species (indicates gram (-) organism, esp E. coli)
    • Urease test –> urease-producing bags (eg. Proteus, klebsiella)
51
Q

acute renal failure (Acute kidney injury) - TYPES

A
  1. Prerenal azotemia
  2. Intrinsic renal failure
  3. postrenal azotemia
52
Q

Prerenal azotemia - urine osmolairty (mOsm/Kg), urine Na+ meq/L, FENa, Serum BUN/Cr

A
  • urine osmolairty –> more than 500
  • urine Na+ less than 20
  • FENa less than 1%
  • Serum BUN/Cr >20
53
Q

Intrinsic renal failure - due to

A
  • acute tubular necrosis or ischemia/toxins

- less commonly due to acute glomerulonephritis (RPGN, hemolytic uremic syndrome) or acute interstitial nephritis

54
Q

intrinsic failure - urine osmolairty (mOsm/Kg), urine Na+ meq/L, FENa, Serum BUN/Cr

A
  • urine osmolairty –> less than 350
  • urine Na+ more than 40
  • FENa more than 2%
  • Serum BUN/Cr less than 15
55
Q

postrenal azotemia - urine osmolairty (mOsm/Kg), urine Na+ meq/L, FENa, Serum BUN/Cr

A
  • urine osmolairty –> less than 350
  • urine Na+ more than 40
  • FENa more than 1% (mild) or 2% (severe)
  • Serum BUN/Cr varies
56
Q

Acute interstitial renal nephritis (tubulointesritital nephritis) - clinical presentation/findings

A 
IT CAN BE ASYMPTOMATIC
1. Fever
2. rash
3. hematuria (casts)
4. costovertebral angle tenderness 
5. pyuria (classically eosinophils) 
6. azotemia
7. oliguria
(days to weeks after the factor) 
RESULTS IN ACUTE RENAL FAILURE
57
Q

causes of Acute interstitial renal nephritis (tubulointesritital nephritis)

A
  1. drugs that act as haptens, inducing hypersensitivity (eg. diuretics, penicillin derivatives, PPIs, sulfonamides, rifampin, NSAID)
  2. Systemic infections (eg. mycoplasma)
  3. Autoimmune diseases (eg. Sjogren syndrome, SLE, sarcoidosis)
58
Q

Acute interstitial renal nephritis (tubulointesritital nephritis) may progress to

A

renal papillary necrosis

59
Q

renal papillary necrosis - symptoms/findings

A
  1. gross hematuria
  2. proteinuria
  3. flank pain
60
Q

causes of renal papillary necrosis

A
  1. Sickle cell disease or trait
  2. acute pyelonephritis
  3. NSAID (or phenacetin)
  4. DM
  5. Acute interstitial renal nephritis
    May be triggered by recent infection or immune stimulus
61
Q

MCC of acute kidney injury in hospitalized patients

A

Acute tubular necrosis

62
Q

Acute tubular necrosis - prognosis

A

can be fatal, esp during initial oligurinc phase

63
Q

Acute tubular necrosis - FENa

A

more than 2%

64
Q

Acute tubular necrosis - key finding

A

granular (muddy brown) casts

65
Q

Acute tubular necrosis - stages

A
  1. inciting event
  2. Maintenance phase - oliguric
  3. Recovery phase - polyuric
66
Q

Acute tubular necrosis - maintenance phase - risk for

A
  1. hyperkalemia
  2. metabolic acidosis
  3. uremia
67
Q

Acute tubular necrosis - Recovery phase - findings

A

BUN and creatinine fall

68
Q

Acute tubular necrosis - recovery phase - risk for

A

hypokalemia

69
Q

Acute tubular necrosis can be caused by …. (groups)

A
  1. ischemic factors

2. nephrotoxic factors

70
Q

Acute tubular necrosis - nephrotoxic factors - mechanism

A

2ry to injury resulting from toxic substance (eg. aminglycosides, radiocontrasts agents, lead, cisplatin), crush injury (myoglobinuria), hemoglobinuria

71
Q

Cast in urine - types

A
  1. RBC casts
  2. WBC casts
  3. Fatty casts (oval fat bodies)
  4. Granular (“muddy brown”) casts
  5. Waxy casts
  6. Hyaline casts
72
Q

RBC casts - seen in

A
  1. glomerulonephritis

2. malignant hypertension

73
Q

WBC cast - seen in

A
  1. tubulointerstitial inflammation
  2. acute pyelonephritis
  3. trasnplant rejection
74
Q

Fatty casts (oval fat bodies) - seen in / associated with

A

Nephrotic syndrome

- Maltese-cross sign under polarized light

75
Q

Granular (“muddy brown”) vs waxy casts - seen in / cells

A

granular –> acute tubular necrosis
waxy –> renal failure
BOTH ACELLULAR

76
Q

Hyaline casts - seen in / contain

A

nonspecific, can be normal finding, often in concentrated urine samples
- protein (acellula)

77
Q

Nomenclature of glomerular disorders - focal (characteristcs and example)

A
  • less than 50% of glumeri are involved

- ex. focal segmental glomerulosclerosis

78
Q

Nomenclature of glomerular disorders - diffuse (characteristcs and example)

A
  • more than 50% of glumeri are involved

- ex. diffuse proliferative glumerulonephritis

79
Q

Nephritic syndrome vs nephrotic syndrome according to mechanism

A

Nephritic syndrome –> GBM disruption

Nephrotic syndrome –> podocyte disruption –> barier impaired

80
Q

Nephritic syndrome - symptoms and findings

A
  1. Hypertension (salt secretion and periorbital edema)
  2. increased BUN and creatinine
  3. oliguria
  4. hematuria (with RBCs in urine)
  5. Proteinuria in Subnehrotic range (in severe cases may be in nephrotic range)
81
Q

Nephritic syndrome - diseases?

A
  1. acute poststreptococcal glomerulonephritis
  2. Rapidly progressive glomerulonephritis
  3. IgA nephropathy (Berger disease)
  4. Alport syndrome
  5. Membranoproliferative glomerulonephritis
  6. Diffuse proliferative glomerulonephritis
82
Q

Nephrotic syndrome - symptoms and findings

A
  1. Massive proteinuria (>3.5g/day) with hypoalbuminemia (pitting edema in soft tissues)
  2. hyperlipidemia (frothy urine with fatty casts)
  3. edema
  4. hypogammaglobulinemia (increased risk of infection)
  5. loss of antithrombin III –> hypercoagulable state
83
Q

Nephrotic syndrome - diseases (and if 1ry or 2ry)

A
  1. focal segmental glomeulosclerosis (1ry or 2ry)
  2. minimal change disease (lipoid nephrosis) (1ry or 2ry)
  3. Membranous nephropathy (membranous glomerulonephritis) (1ry or 2ry)
  4. Amyloidosis (2ry)
  5. Diabetic glomerulonephropathy
84
Q

Nephritic-nephrotic syndrome?

A

severe nephritic syndrome with profound GBM damage that may damages the glomerular filtration charge barrier (if damage to GBM is severe enougj to damage charger barrier)
–> nephrotic-range proteinuria (>3.5g.day) and concominant features of nephrotic syndrome

85
Q

Causes of Nephritic-nephrotic syndrome

A

can occur with any form of nephritic syndrome, but is most common seen with

  1. diffuse proliferative glomerulonephritis
  2. Membranoproliferative glomerulonephritis
86
Q

Nephritic vs nephrotic vs Nephritic-nephrotic syndrome according to protein excreted per day

A

nephritic: Proteinuria in Subnehrotic range (less than in severe casees may be in nephrotic range
nephrotic: Massive proteinuria (>3.5g/day) with hypoalbuminemia
Nephritic-nephrotic syndrome: nephrotic-range proteinuria (>3.5g.day)

87
Q

Acute poststreptococcal glomerulonephritis - age / when

A

Most frequently seen in children (may also occur in adults)

- 2-4 weeks after A streptococcal infection of of skin (impetigo) or pharynx

88
Q

Acute poststreptococcal glomerulonephritis - treatment

A

resolves spontaneously

89
Q

Acute poststreptococcal glomerulonephritis - lab

A
    • strep titers/serologies
  2. low complement levels due to consumption
  3. LM: glomeruli enlarged and hypecellular
  4. IF: (starry sky) granular appearance (lumpy-bumpy) due to IgG, IgM and C3 deposotio along GBM and mesangium
  5. EM: subepithelial immune complex (IC) humbs
90
Q

causes of Rapidly progressive (crescentic) glomerulonephritis

A

several diseases processes may result in this pattern

  1. Goodpasture - anti-GBM + anti alveolar BM
  2. Granulomatosis with polyangiitis (Wegener) - PR3-ANCA/c-ANCA
  3. Microscopic polyangitis, Churg strauus - MPO-ANCA/p-ANCA
  4. poststreptococcal glomerulonephritis
  5. Diffuse proliferative glomerulonephritis
91
Q

Rapidly progressive (crescentic) glomerulonephritis - image

A

LM: crescent moon shape –> consist of fibrin and plasma proetins (eg. C3b) with glomerular parietal cells, monocytes, macrophages
IF: a. Goodpasture –> linear b. wegener, Microscopic polyangitis –> negative IF (Pauci-immune –> no IG/C3 deposotion) c. if PSGN or Diffuse proliferative glomerulonephritis –> granular

92
Q

Rapidly progressive (crescentic) glomerulonephritis - treatment / prognosis

A

emergent plasmapheresis

poor prognosis

93
Q

Diffuse proliferative glomerulonephritis - mechanism

A

due to SLE or membranoproliferative glomerulonephritis

94
Q

Diffuse proliferative glomerulonephritis - image

A

LM - wire looping of capillaries
EM: subendothelial and sometimes intramembranous IgG-based ICs often with C3 deposotion
IF: granular

95
Q

IgA nephrpathy (Berger disasee) -mechanism/presentation

A

episodic gross hematuria that occurs concurrently with respiratory or GI tract infection (IgA is secreted by mucosal linings) –> IgA complex
RENAL PATHOLOGY OF HENOCH-SCHONLEIN PURPURA

96
Q

IgA nephrpathy (Berger disasee) - image

A

LM - mesangial proliferation
EM - mesangial IC depositis
IF - IgA-based IC deposits in mesangium

97
Q

Alport syndrome - mechanism / mode of inheritance

A

Mutation in type IV collagen –> thinning and splitting of glomerular basement membrane
MC X-linked dominant

98
Q

Alport syndrome - manifestation

A
  1. Eye problem (eg. retinopathy, lens dislocation)
  2. glomerulonephritis –> isolated hematuria
  3. sensorineural deafness
99
Q

Alport syndrome - image

A

Basket-weave” appearance on EM

100
Q

Mebranoproliferative glomerulonephritis (MPGN) - mechanism

A 
type 1 --> 2ry to hepatitis B or C infection, May also be idiopathic 
type 2 (dense deposit disease) --> associated with C3 nephritic factor (autoantibody that stabilize C3 convertase) --> low serum C3 levels
101
Q

Mebranoproliferative glomerulonephritis (MPGN) - prognosis

A

poor response to steroids –> progress to chronic renal failure

102
Q

Mebranoproliferative glomerulonephritis (MPGN) type I - image

A

subendothelial immune complex (IC) deposits with granular IF
tram track appearance on PAS stain and H&E stain due to GBM splitting caused by mesangial ingrowth

103
Q

Mebranoproliferative glomerulonephritis (MPGN) type I vs type to according to location of deposits

A

type 1 –> subendothelial

type 2 –> intramembranous

104
Q

MCC of nephrotic syndrome in children / treatment

A

Minimal change disease (lipoid nephrosis)

- excellent response to corticosteroids

105
Q

Minimal change disease (lipoid necrosis) - image

A

LM - normal glomeruli, lipid may be seen in PCT cells
IF - normal
EM - effacement of foot process

106
Q

MCC of nephrotic syndrome in African and Hispanics

A

Focal segmental glomerulosclerosis

107
Q

causes of focal segmental glomerulosclerosis

A
  1. Can be 1ry (idiopathic)
  2. 2ry to other conditions –> a. HIV infection b. Sickle cell anemia c. heroin abuse d. massive obesity
    e. interferon treatment f. chronic kidney disease due to congenital malformations
108
Q

focal segmental glomerulosclerosis - course and treatment

A

may progress to chronic renal disease

1ry disease has incosistent response to steroids

109
Q

focal segmental glomerulosclerosis - image

A

LM - segmental sclerosis and hyalinosis
IF - often (-), but may be + for nonspecific focal deposits of IgM, C3, C1…
EF - effacement of ffot process similar to minimal

110
Q

MC cause of 1ry nephrotic syndrome in Caucasian adults

A

Membranous nephropathy (membranous glomerulonephritis)

111
Q

causes of Membranous nephropathy (membranous glomerulonephritis)

A
  1. primary (antibodies to phospholypase A2 receptor)

2. 2ry to: a. drugs (eg. NSAIDs, penicillamine) b. infections (HBV, HCV) c. SLE d. solid tumors

112
Q

causes of Membranous nephropathy (membranous glomerulonephritis) - course and treatment

A

may progress to chronic renal disease

1ry disease has poor response to steroids

113
Q

Membranous nephropathy (membranous glomerulonephritis) - image

A

LM - diffuse capillary and BM thickenning
IF - granular (immune complex)
EM - “spike and done” appearance with subepithelial deposits

114
Q

nephrotic syndrome - amyloidosis - image

A

LM - congo red stain shows apple green birefringence under polairzed light due to amyloid deposition in the mesangium

115
Q

MCC of end-stage renal disease in US

A

Diabetic glomerulonephropathy

116
Q

Diabetic glomerulonephropathy - mechanism

A

Nonenzymatic glycosylation of GBM –> increased permeability, thickening
Nonenzymatic glycosylation of efferent arterioles –> increased GFR –> mesangial expansion

117
Q

HCV, HBV nephritis - types

A

nephrotic –> Membraous nephropathy (membranous glomerulonephritis)
nephritic –> membranoproliferative glomerulonephritis

118
Q

Lupus nephritis - types

A

nephritic - diffuse proliferative glomerulonephritis

nephrotic - membranous glomerulonephritis

119
Q

MC nephropathy worldwide

A

IgA nephropathy (Berger disease)

120
Q

glomerular disease with subepithelial deposits

A
  1. Acute poststreptococcal glomerulonephritis

2. Membranous nephropathy (membranous glomerulonephritis)

LUNG + RENAL STEP 2 (5 decks)

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